Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy. - Wikidata - wikimedia - TriplyDB

Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy.

Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy.

http://www.wikidata.org/entity/Q36932490

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Extracellular signal-regulated kinases 1/2 as regulators of cardiac hypertrophy Oxidative stress and epigenetic regulation in ageing and age-related diseases The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy Heart failure: advanced development in genetics and epigenetics Emerging roles for histone deacetylases in pulmonary hypertension and right ventricular remodeling (2013 Grover Conference series)Selumetinib, an Oral Anti-Neoplastic Drug, May Attenuate Cardiac Hypertrophy via Targeting the ERK Pathway In vivo imaging of histone deacetylases (HDACs) in the central nervous system and major peripheral organs.Selective inhibition of class I but not class IIb histone deacetylases exerts cardiac protection from ischemia reperfusion.Class I HDACs regulate angiotensin II-dependent cardiac fibrosis via fibroblasts and circulating fibrocytes.A novel role for histone deacetylase 6 in the regulation of the tolerogenic STAT3/IL-10 pathway in APCs.Protein expression, characterization and activity comparisons of wild type and mutant DUSP5 proteins Lactosylceramide promotes hypertrophy through ROS generation and activation of ERK1/2 in cardiomyocytes.Selective HDAC inhibition for the disruption of latent HIV-1 infection.Non-sirtuin histone deacetylases in the control of cardiac aging Histone Deacetylase 3 Is Required for Efficient T Cell Development.Dual Specificity Phosphatase 5 Is Essential for T Cell Survival Histone Modification of Nedd4 Ubiquitin Ligase Controls the Loss of AMPA Receptors and Cognitive Impairment Induced by Repeated Stress.DUSP8 Regulates Cardiac Ventricular Remodeling by Altering ERK1/2 Signaling.Histone deacetylation contributes to low extracellular superoxide dismutase expression in human idiopathic pulmonary arterial hypertension.Heart failure-specific changes in protein kinase signalling.Targeting cardiac fibroblasts to treat fibrosis of the heart: focus on HDACs.Epigenetic regulation and heart failure.Keeping up the balance: role of HDACs in cardiac proteostasis and therapeutic implications for atrial fibrillation.Regulation of cardiac hypertrophy and remodeling through the dual-specificity MAPK phosphatases (DUSPs).Transcriptional repression of ER through hMAPK dependent histone deacetylation by class I HDACs.DNA methylation regulated gene expression in organ fibrosis.DUSP5 functions as a feedback regulator of TNFα-induced ERK1/2 dephosphorylation and inflammatory gene expression in adipocytes Class I HDACs control a JIP1-dependent pathway for kinesin-microtubule binding in cardiomyocytes.Inhibition of HDAC3 prevents diabetic cardiomyopathy in OVE26 mice via epigenetic regulation of DUSP5-ERK1/2 pathway.Food Bioactive HDAC Inhibitors in the Epigenetic Regulation of Heart Failure The Crosstalk between Acetylation and Phosphorylation: Emerging New Roles for HDAC Inhibitors in the Heart

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P2860

Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy.

http://www.wikidata.org/entity/Q36932490

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2013 nî lūn-bûn

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Signal-dependent repression of ...... and cardiomyocyte hypertrophy.

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Signal-dependent repression of ...... and cardiomyocyte hypertrophy.

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Signal-dependent repression of ...... and cardiomyocyte hypertrophy.

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PNAS.1301509110

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Proceedings of the National Academy of Sciences of the United States of America

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Signal-dependent repression of ...... and cardiomyocyte hypertrophy.

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P2093

Brian G Reid

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Brooke C Harrison

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Edward B Holson

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Florence F Wagner

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Mark Y Jeong

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Michael F Wempe

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Timothy A McKinsey

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P2860

Heart Disease and Stroke Statistics--2010 Update: A Report From the American Heart Association

Specific inactivation and nuclear anchoring of extracellular signal-regulated kinase 2 by the inducible dual-specificity protein phosphatase DUSP5

Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5

Histone deacetylase (HDAC) inhibitors attenuate cardiac hypertrophy by suppressing autophagy

Lysine acetylation targets protein complexes and co-regulates major cellular functions

Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy.

A calcineurin-dependent transcriptional pathway for cardiac hypertrophy

DUSP6 (MKP3) null mice show enhanced ERK1/2 phosphorylation at baseline and increased myocyte proliferation in the heart affecting disease susceptibility

Histone deacetylases facilitate sodium/calcium exchanger up-regulation in adult cardiomyocytes

Heart disease and stroke statistics--2012 update: a report from the American Heart Association

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9806-9811

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10.1073/PNAS.1301509110

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24

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110

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Bradley S. Ferguson

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2013-05-29T00:00:00Z

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236968491

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23720316

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3683796

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